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Biomedical subjects

R J Joehl

Publications and source records attributed to R J Joehl.

At least 55 records · Page 3Linked to original sources
PubMed1991

Bile exclusion from the gut exacerbates acute pancreatitis caused by pancreatic duct obstruction in rats.

Acute pancreatic duct obstruction causes hyperamylasemia and mild pancreatic inflammation. We hypothesized that bile exclusion from the gut, which stimulates pancreatic secretion, exacerbates acute pancreatitis caused by pancreatic duct obstruction. Rats were surgically prepared with gastric, duodenal, bile, and pancreatic fistula catheters and a jugular vein catheter. After a 4-day recovery, groups of rats (a) served as controls, (b) had complete pancreatic duct obstruction for 6 h, or (c) had bile excluded from the gut for 24 h and then, during the final 6 h, complete pancreatic duct obstruction. Plasma amylase was measured, and all rats were euthanized at the end of experiments. Each pancreas was excised and weighed, and portions were fixed in formalin and glutaraldehyde. In blind fashion, each pancreas was examined under light microscopy and assigned a pancreatitis score based on presence of edema and severity of acinar cell changes and inflammation. Acute pancreatic duct obstruction was associated with increased pancreas weight, hyperamylasemia, and elevated pancreatitis score; moderate acinar cell vacuoles, which were observed in the cytoplasm near the basolateral membrane, and loss of microvilli were noted with electron microscopy. Bile exclusion from the gut exacerbated the acute pancreatitis caused by pancreatic duct obstruction; acinar cell distortion and destruction, as well as marked inflammation, were seen microscopically. These observations suggest that the absence of intestinal bile contributes to the pathogenesis of acute pancreatitis associated with pancreatic duct obstruction.

Acute Disease↗
PubMed1990

Gastrointestinal lymphoma. A case for primary surgical resection.

The cases of 42 consecutive patients with primary gastrointestinal lymphoma were reviewed to compare the risks and outcomes of different primary treatment modalities. Among patients with localized disease (stages I and II), 12 underwent complete tumor resection and 6 underwent radiation therapy; 5-year survival was 82% and 50%, respectively. Among patients with disseminated disease (stages III and IV), 6 underwent resection of the primary tumor followed by chemotherapy and 18 were treated with radiation and chemotherapy; 5-year survival was 81% and 6%, respectively. Five patients who did not undergo surgical resection before radiation therapy or chemotherapy developed severe life-threatening complications from their primary tumor. Surgical resection before the administration of other therapy should be performed when the patient is considered to be a surgical candidate and resection of the primary tumor is deemed feasible.

Adolescent↗
PubMed1990

Does somatostatin analogue prevent experimental acute pancreatitis?

Because somatostatin is a potent inhibitor of pancreatic secretion, we hypothesized that pretreatment with somatostatin analogue octreotide (SMS 201-995) might prevent cerulein-induced edematous pancreatitis. We studied 18 rats prepared with jugular vein catheters. The following agents were administered intravenously to groups of four rats for 6 hours: 1 mL/h (control) crystalloid solution; 1-microgram/kg bolus then 1 microgram/kg per hour of octreotide; and 5 micrograms/kg per hour of cerulein; also, in a fourth group of six rats, octreotide and cerulein were administered simultaneously. At the end of experiments, blood was drawn for plasma amylase determinations; rats were killed and pancreata were examined. Supramaximal cerulein administration to conscious rats induced hyperamylasemia and edematous pancreatitis, confirming previous observations; in both groups of rats receiving cerulein, there was prominent interstitial edema, acinar vacuolization, and mild-to-moderate acute inflammation. While octreotide pretreatment of rats with cerulein-induced acute pancreatitis was associated with a lesser increase of wet pancreas weight and plasma amylase concentration, there was little overall benefit of octreotide pretreatment in this form of experimental acute pancreatitis.

Acute Disease↗
PubMed1990

Cholecystokinin antagonist prevents hyperamylasemia and improves pancreatic exocrine function in cerulein-induced acute pancreatitis.

Supramaximal cerulein administration induces acute pancreatitis, which markedly impairs pancreatic secretion in conscious rats. We hypothesized that pretreatment with the potent cholecystokinin antagonist, L-364,718, improves the pancreatic secretory impairment associated with cerulein-induced acute pancreatitis. Rats were surgically prepared with gastric, duodenal, bile, and pancreatic fistulas and jugular vein catheters. On postoperative day 4, groups of rats were administered (a) L-364,718 1 mg/kg intraduodenally, (b) cerulein 5 micrograms/kg/h for 6 h intravenously, (c) L-364,718 1 mg/kg intraduodenally followed by cerulein 5 micrograms/kg/h for 6 h intravenously, and (d) safflower oil carrier intraduodenally. On postoperative day 5, we studied cholecystokinin (CCK)-stimulated pancreatic secretion. Plasma amylase was measured at the time of surgery and at the conclusion of experiments on postoperative days 4 and 5. The duodenally administered CCK antagonist had no effect, 24 h later, on CCK-evoked protein secretion and prevented the pancreatic exocrine impairment and hyperamylasemia caused by supramaximal cerulein administration. These observations suggest that cerulein-induced acute pancreatitis is mediated by a CCK-receptor mechanism.

Acute Disease↗
PubMed1990

Acute edematous pancreatitis impairs pancreatic secretion in rats.

There are few observations of in vivo pancreatic secretory changes that accompany acute pancreatitis. We hypothesized that acute pancreatitis impairs pancreatic exocrine function. We developed a conscious-rat experimental preparation with gastric, duodenal, bile, and pancreatic fistulas. We studied cholecystokinin-stimulated pancreatic secretion in conscious rats before and after inducing acute pancreatitis with supramaximal administration of caerulein--5 micrograms/kg/hr intravenously for 6 hours. Marked hyperamylasemia developed in all rats immediately after administration of caerulein. Basal and cholecystokinin-stimulated pancreatic juice flow and protein (enzyme) secretion decreased significantly 24 hours after acute pancreatitis was induced even though plasma amylase returned to basal levels. We conclude that acute pancreatitis markedly impairs pancreatic secretion.

Acute Disease↗
PubMed1990

Rates of morbidity and mortality after closure of loop and end colostomy.

The purported ease and safety of closure of loop colostomy are cited as reasons for avoiding end colostomy, with or without resection. However, data comparing the complications of loop colostomy closure and end colostomy takedown and anastomosis are sparse. We analyzed data from 93 consecutive colostomy closures, of which 62 were loop and 31 were end colostomies. The two groups were comparable with respect to age, the underlying disease and risk factors, such as coronary artery disease, diabetes, hypertension, steroid dependence, hypoalbuminemia and smoking. Closure of end colostomies took longer and was associated with more loss of blood than closure of loop colostomies. However, the mortality rates for closure of loop (4.8 per cent) and end (3.2 per cent) colostomies were not significantly different. The complication rates were identical (16 per cent). Although none of the other risk factors were associated with increased rates of mortality or morbidity, the detrimental effects of steroid dependence and preoperative hypoalbuminemia were striking. All four of the deaths and 60 per cent of the complications occurred in patients with steroid dependence or hypoalbuminemia, or both. The rates of wound infection after primary or secondary closure of the stoma site were not significantly different. We concluded that loop colostomy closure is not associated with fewer complications than closure of end colostomy, even though the latter takes longer and is more difficult. Hypoalbuminemic and steroid-dependent patients should undergo colostomy closure with caution, if at all. Primary closure of the stomal site is safe and reduces the length of hospital stay.

Adrenal Cortex Hormones↗
PubMed1989

A foregut carcinoid tumor causing Zollinger-Ellison syndrome.

A patient had severe peptic ulcer disease complicated by gastric outlet obstruction and choledochoduodenal fistula. Serum gastrin levels were elevated preoperatively to 340 ng/L. A 1.5-cm histologically benign carcinoid tumor of the antrum of the stomach was found at surgery, and surgical resection of the tumor resulted in normalization of serum gastrin levels and amelioration of the peptic acid diathesis. The patient remains asymptomatic at one year. Immunohistochemical staining demonstrated that the carcinoid indeed contained gastrin along with chromogranin, cholecystokinin, and neuron-specific enolase. This is a case of Zollinger-Ellison syndrome caused by a benign foregut carcinoid (gastric carcinoid-gastrinoma).

Aged↗
PubMed1989

Percutaneous cholecystostomy in the diagnosis and treatment of acute cholecystitis in the high-risk patient.

We performed percutaneous cholecystostomy in 22 critically ill patients with suspected acute cholecystitis. This procedure accurately diagnosed acute cholecystitis in 17 of these 22 patients and excluded the diagnosis in the other 5 patients. Moreover, percutaneous cholecystostomy stabilized the conditions of 16 of the 17 patients with acute cholecystitis, allowing elective surgery in 8 patients and effectively treating 8 patients who never became surgical candidates. Percutaneous cholecystostomy and bile cultures are useful in the diagnosis and treatment of acute cholecystitis and should be performed in critically ill patients with clinical, laboratory, and radiologic evidence of acute cholecystitis and an excessive risk for cholecystectomy.

Acute Disease↗
PubMed1988

Treatment of anastomotic leakage following low anterior colon resection.

Four hundred five consecutive cases of low anterior colon resection were studied to determine the best treatment of anastomotic leak. The triad of fever, leukocytosis, and pelvic pain was present in 15 of the 16 cases with leaks. Four (25%) of the 16 patients died. Eleven were managed by proximal decompression and drainage; four died (36%). Three patients underwent takedown of the anastomosis, end colostomy, and distal closure or exteriorization; none died. Neither of the two patients who had drainage alone died. Anastomotic leakage accounted for two thirds of the deaths in this series. Recognition of the clinical triad of fever, leukocytosis, and pelvic pain could lead to earlier diagnosis and improved outcome. Our data suggest that a procedure that includes takedown of the anastomosis, end colostomy, and closure of the rectum is the most efficacious treatment of anastomotic leakage after low anterior colon resection.

Anastomosis, Surgical↗
PubMed1987

Posterior sagittal anorectoplasty for adults. A sphincter-saving operation.

We performed posterior sagittal anorectoplasty to treat two adult patients. One patient had an idiopathic stricture extending from the proximal sigmoid colon to the anus. The second patient was born with a high imperforate anus and, following a pull-through procedure as an infant, remained totally incontinent of feces. Both patients now have excellent fecal continence following this operation. The posterior sagittal anorectoplasty may be used to preserve rectal continence in selected adults.

Adult↗
PubMed1987

One-stage resection and anastomosis in the management of colovesical fistula.

Thirty-four patients with colovesical fistulas seen over a recent 10 year period were reviewed. Diverticulitis was the most common cause of colovesical fistula, accounting for 71 percent of patients in our series. The majority of patients present electively, and most have urinary tract complaints. In those patients in our study who presented with systemic infection, urinary obstruction was present in 70 percent. Although proctosigmoidoscopy and barium enema examination are essential in the preoperative assessment, cystoscopy is the most useful test in suggesting or confirming the diagnosis of colovesical fistula. Intravenous urography is not necessary in the evaluation of these patients. The surgical treatment depends on the cause of the fistula. For patients with an inflammatory cause of the fistula, one-stage operative treatment is associated with low morbidity and decreased length of stay compared with operative treatment in more than one stage. In the presence of severe inflammation or inadequate bowel preparation, two-stage operative treatment is safe and effective. Operations in three stages for colovesical fistula are not indicated. The primary objectives in the management of colovesical fistulas due to unresectable malignancy are relief of intestinal and urinary obstruction and fecal diversion. Resection of the malignancy should be performed whenever possible.

Adult↗
PubMed1986

External duodenal fistula. Causes, complications, and treatment.

We reviewed records of 18 patients with external duodenal fistula. Fourteen patients developed duodenal fistulas following an operation, two following abdominal trauma, and two as a complication of other diseases. Copious drainage of intestinal juice from the abdomen was the most common presenting sign. Contrast fistulography, upper gastrointestinal tract roentgenography, and T-tube cholangiography were useful diagnostic studies. Nine patients were treated nonoperatively; nine patients required at least one operation. Complications occurred frequently; of special interest were three patients who developed postoperative acute cholecystitis. Six patients died (33% mortality). Factors associated with mortality were advanced age (greater than 65 years), uncontrolled infection and multiple organ failure, high-output fistula, malnutrition, delay in diagnosis (more than three days), and multiple reoperations to treat the fistula or complications. External duodenal fistula continues to be a life-threatening problem whether it is postoperative, posttraumatic, or secondary to a disease process.

Abdominal Injuries↗
PubMed1986

Pancreatic polypeptide inhibits amylase release by rat pancreatic acini.

Pancreatic polypeptide (PP), a mammalian islet cell peptide, is released after a meal. Exogenously administered PP in physiologic doses inhibits cholecystokinin and secretin-stimulated pancreatic secretion in vivo. Whether PP acts directly on exocrine pancreatic cells is unknown. We studied the effects of PP on dispersed acini prepared from rat pancreas. Amylase release was determined after 30-min incubations of pancreatic acini with octapeptide of cholecystokinin (OP-CCK), secretin, and PP. The response to OP-CCK was augmented by secretin. PP decreased optimal amylase release evoked by OP-CCK and OP-CCK plus secretin. These observations demonstrate that PP acts directly on pancreatic cells to reduce acinar cell amylase release evoked by potent secretagogues.

Amylases↗
PubMed1986

Characteristics of inhibition of pancreatic secretion by the beta-adrenergic agonist, terbutaline.

This study was performed to characterize the inhibitory effects of terbutaline on pancreatic secretion. In experiments with pancreatic fistula dogs, intravenously administered terbutaline significantly reduced pancreatic juice volume, bicarbonate concentration, bicarbonate output, and protein output evoked by secretin or the octapeptide of cholecystokinin but had no effect on protein concentration. Subcutaneously administered terbutaline significantly reduced meal-stimulated pancreatic juice volume, bicarbonate concentration, bicarbonate output, and protein output and increased protein concentration in a dose-related manner. In other experiments, terbutaline had no effect on amylase release from dispersed guinea pig pancreatic acini. These observations suggest that the primary effect of terbutaline on the in vivo exocrine pancreas is inhibition of water and bicarbonate secretion; reduced output of pancreatic protein may be secondary to decreased flow of pancreatic juice.

Amylases↗
PubMed1985

Inhibition of human pancreatic secretion by terbutaline as a potential agent for treating patients with pancreatic fistula.

We studied the effects of terbutaline on secretin-stimulated duodenal juice output in six healthy volunteers. When administered intravenously to healthy volunteers, terbutaline significantly inhibited secretin-stimulated output of duodenal juice and bicarbonate. After administration of terbutaline to one patient with an external pancreatic fistula, daily output of pancreatic juice decreased and the fistula closed. Significant side effects were not observed. These observations suggest that terbutaline inhibits human pancreatic secretion. Terbutaline may be useful in treating patients with external pancreatic fistula.

Adult↗
PubMed1984

Obstructive jaundice caused by hepatocellular carcinoma.

Hepatocellular carcinoma can be complicated by obstructive jaundice with tumor growing into the extrahepatic bile duct. This complication is an autopsy finding in most reported cases and, rarely, is recognized ante mortem. We report two patients with hepatocellular carcinoma who presented initially with obstructive jaundice. Clotted blood and tumor, which caused bile duct obstruction, was removed operatively and the biliary tract was drained in both patients. We conclude that blood clot and fleshy debris removed from the common bile duct at operation for obstructive jaundice suggests the possibility of hepatocellular carcinoma; the differential diagnosis of jaundice and fever in patients known to have hepatocellular carcinoma should include intrabiliary tumor causing obstruction and cholangitis; and the association of obstructive jaundice and hepatocellular carcinoma may occur more often than previously recognized.

Adolescent↗
PubMed1984

Opioid drugs cause bile duct obstruction during hepatobiliary scans.

Hepatobiliary scans using Tc-IDA are reliable in making the diagnosis of acute cholecystitis. Commonly, opioid drugs are administered in patients with acute cholecystitis to relieve pain. Opioid drugs cause biliary sphincter spasm. Whether these drugs adversely affect hepatobiliary scans is unknown. We studied 13 healthy volunteer subjects, performing three hepatobiliary scans in each one. Scans were performed without opioid drugs and 30 minutes after intramuscularly administered meperidine, morphine, hydroxyzine, hydroxyzine plus meperidine, butorphanol, and nalbuphine. Opioid drugs markedly delayed clearance of Tc-IDA from the common bile duct, simulating common bile duct obstruction. Hydroxyzine alone caused an insignificant delay. We have concluded that opioid drugs cause bile duct obstruction in healthy persons. If opioid drugs are administered before a diagnostic hepatobiliary scan, delayed clearance of Tc-IDA from the common bile duct might lead to an erroneous diagnosis and indicate a potentially unnecessary common bile duct exploration. Opioid drugs should not be administered for several hours before a diagnostic hepatobiliary scan.

Acute Disease↗